The AcMYB15-AcWRKY24 module coordinates lignin and salicylic acid accumulation during kiwifruit resistance to bacterial canker

Plants coordinate phenylpropanoid metabolism across different tissues to defend against pathogens, but the underlying transcriptional mechanisms remain unclear. Here, we identify the kiwifruit transcription factor AcMYB15 as a regulator that lignin deposition and salicylic acid (SA) accumulation, conferring bacterial canker resistance in kiwifruit through a tissue-specific regulatory module during  Pseudomonas syringae pv. actinidiae (Psa) infection. In leaves, AcMYB15 directly binds to the CAACCC motif in the AcPAL1 promoter to activate its transcription, promoting localized lignin accumulation. In stems, which are the primary conduits for systemic Psa colonization, AcMYB15 forms a protein complex with the stem-enriched transcription factor AcWRKY24. Formation of the AcMYB15-AcWRKY24 protein complex enhanced transcriptional activation of the stem-prevalent AcPAL2 by strengthening its DNA-binding preferences for the CAACCA motif. Functional characterization indicates that AcPAL1 and AcPAL2 exert distinct defensive roles: AcPAL1 overexpression primarily leads to increased lignin deposition, whereas AcPAL2 overexpression predominantly enhances SA accumulation. Therefore, the AcMYB15-AcWRKY24 synergistic module provides a coordinated defense mechanism in the stem by simultaneously promoting lignin deposition and SA accumulation, thereby conferring enhanced resistance to bacterial canker. Our study uncovers a two-tiered transcriptional mechanism that coordinately regulates the tissue-specific accumulation of lignin and SA during Psa infection. These findings provide a solid theoretical basis and potential genetic resources for the genetic improvement and molecular breeding of disease-resistant fruit crops.